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dc.contributor.authorSokolova, Marinaen_US
dc.contributor.authorSjaastad, Ivaren_US
dc.contributor.authorLouwe, Maria Corneliaen_US
dc.contributor.authorAlfsnes, Katrineen_US
dc.contributor.authorAronsen, Jan Magnusen_US
dc.contributor.authorZhang, Lilien_US
dc.contributor.authorHaugstad, Solveig Bjærumen_US
dc.contributor.authorBendiksen, Bård Andreen_US
dc.contributor.authorØgaard, Jonasen_US
dc.contributor.authorBliksøen, Marteen_US
dc.contributor.authorLien, Egilen_US
dc.contributor.authorBerge, Rolf Kristianen_US
dc.contributor.authorAukrust, Pålen_US
dc.contributor.authorRanheim, Trineen_US
dc.contributor.authorYndestad, Arneen_US
dc.PublishedSokolova M, Sjaastad I, Louwe MC, Alfsnes K, Aronsen JM, Zhang L, Haugstad SB, Bendiksen BA, Øgaard J, Bliksøen M, Lien E, Berge RK, Aukrust P, Ranheim T, Yndestad A. NLRP3 inflammasome promotes myocardial remodeling during diet-induced obesity. Frontiers in Immunology. 2019;10:1621eng
dc.description.abstractBackground: Obesity is an increasingly prevalent metabolic disorder in the modern world and is associated with structural and functional changes in the heart. The NLRP3 inflammasome is an innate immune sensor that can be activated in response to endogenous danger signals and triggers activation of interleukin (IL)-1β and IL-18. Increasing evidence points to the involvement of the NLRP3 inflammasome in obesity-induced inflammation and insulin resistance, and we hypothesized that it also could play a role in the development of obesity induced cardiac alterations. Methods and Results: WT, Nlrp3−/−, and ASC−/− (Pycard−/−) male mice were exposed to high fat diet (HFD; 60 cal% fat) or control diet for 52 weeks. Cardiac structure and function were evaluated by echocardiography and magnetic resonance imaging, respectively. Whereas, NLRP3 and ASC deficiency did not affect the cardiac hypertrophic response to obesity, it was preventive against left ventricle concentric remodeling and impairment of diastolic function. Furthermore, whereas NLRP3 and ASC deficiency attenuated systemic inflammation in HFD fed mice; long-term HFD did not induce significant cardiac fibrosis or inflammation, suggesting that the beneficial effects of NLRP3 inflammasome deficiency on myocardial remodeling at least partly reflect systemic mechanisms. Nlrp3 and ASC (Pycard) deficient mice were also protected against obesity-induced systemic metabolic dysregulation, as well as lipid accumulation and impaired insulin signaling in hepatic and cardiac tissues. Conclusions: Our data indicate that the NLRP3 inflammasome modulates cardiac concentric remodeling in obesity through effects on systemic inflammation and metabolic disturbances, with effect on insulin signaling as a potential mediator within the myocardium.en_US
dc.rightsAttribution CC BYeng
dc.subjectcardiac remodelingeng
dc.subjecthigh-fat dieteng
dc.titleNLRP3 inflammasome promotes myocardial remodeling during diet-induced obesityen_US
dc.typePeer reviewed
dc.typeJournal article
dc.rights.holderCopyright 2019 Sokolova, Sjaastad, Louwe, Alfsnes, Aronsen, Zhang, Haugstad, Bendiksen, Øgaard, Bliksøen, Lien, Berge, Aukrust, Ranheim and Yndestad.
dc.source.journalFrontiers in Immunology

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